Fighting the Blues with Greens?

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Natural monoamine oxidase enzyme inhibitors in fruits and vegetables may help explain the improvement in mood associated with switching to a plant-based diet.

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Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

Why does frequent consumption of vegetables appear to cut one’s odds of depression by more than half? And, by more frequent, they mean eating vegetables not three or more times a day, but just three or more times a week. But, even that seemed to cut the odds of developing depression by 60%, after controlling for a long list of variables.

In the 2012 study that found that eliminating animal products improved mood within two weeks, the researchers blamed arachidonic acid—primarily in chicken and eggs, which may adversely impact mental health via a cascade of brain inflammation. But, better moods on plant-based diets could also be from the good stuff in plants—a class of phytonutrients that crosses the blood-brain barrier into our heads. This recent review in the journal Nutritional Neuroscience suggests that eating lots of fruits and vegetables may present “a noninvasive, natural, and inexpensive therapeutic means to support a healthy brain.” Yeah, but how?

Well to understand the latest, we need to understand the underlying biology, the so-called monoamine theory of depression—the thought that depression may arise out of a chemical imbalance in the brain. Here’s the oversimplified version. One of the ways the billions of nerves in our brain communicates with one another is through chemical signals called neurotransmitters. Here’s the end of one nerve, and the beginning of another.

This is what it actually looks like under a microscope. Note the two nerve cells don’t actually touch; there’s a physical gap between them. To bridge that gap, when one nerve wants to tap the other on the shoulder, it releases chemicals into that gap, including three monoamines, serotonin, dopamine, and norepinephrine. These neurotransmitters then float over to the other nerve, to get its attention. The first nerve then sucks them back up, to be reused the next time it wants to talk. But, it’s also constantly manufacturing more, and an enzyme—monoamine oxidase—is constantly chewing them up to maintain just the right amount.

The way cocaine appears to work is by acting as a monoamine reuptake inhibitor. It blocks the first nerve from sucking back up those three chemicals, and so, there’s this constant tapping on the shoulder, this constant signaling to the next nerve. Amphetamines work in the same way, but also increase monoamine release. Ecstasy works like speed, but just causes comparatively more serotonin release.

After a while, the next nerve may be like, enough already, and downregulate its receptors to turn down the volume. It puts in earplugs. So, you need more and more of the drug to get the same effect. And then, when you’re not on the drug, you may feel crappy—because normal volume transmission just isn’t getting through as much.

Antidepressants are thought to work along similar mechanisms. People who are depressed appear to have elevated levels of monoamine oxidase in their brain. That’s the enzyme that breaks down those neurotransmitters. And so, if you have too much of that enzyme in critical parts of your brain—the black circles are the levels in the brains of depressed individuals, and white circles that of the healthy individuals. If your levels of your neurotransmitter-eating enzyme is elevated, then your levels of neurotransmitters drops, and you become depressed, or so the theory goes.

So, a number of different classes of drugs have been developed. The tricyclic antidepressants—named because they have three rings, like a tricycle—appear to block norepinephrine and dopamine reuptake. And so, even though your enzymes may be eating these up at an accelerated rate, what gets released sticks around longer. Then, there came the SSRIs, like Prozac—the selective serotonin reuptake inhibitors. Now, you can know what that means—it just blocks the reuptake of serotonin.

Then, there are drugs that just block the reuptake of norepinephrine. Or, more dopamine. Or, the opposite. But, if the problem is too much high levels of monoamine oxidase, why not just block the enzyme? Make a monoamine oxidase inhibitor. And, of course they did. But, they’re considered drugs of last resort because of serious side effects—not the least of which is the dreaded “cheese effect,” where eating certain foods (like certain cheeses) while on the drug can have potentially fatal consequences. If only there were a way to tamp down the activity of this enzyme, without the whole bleed-into-your-brain thing, and die thing.

Well, now we can finally talk about the latest theory as to why fruits and vegetables may improve our mood. There are inhibitors of that depression-associated enzyme in various plants. There are phytonutrients in spices, such as cloves, oregano, cinnamon, nutmeg. But, people don’t eat enough spices to get enough into the brain. This dark green leafy has a lot, but its name is tobacco—which may actually be one of the reasons cigarettes make smokers feel so good.

Okay, but what if you don’t want brain bleeds or lung cancer? Well, there is a phytonutrient found in apples, berries, and grapes, and kale, onions, and green tea that may indeed affect our brain biology enough to improve our mood.

Please consider volunteering to help out on the site.

Images thanks to practicalowl and gloom via flickr, and Mouagip, Nrets, Dake, ThePallanz, and Savant-fou via Wikimedia. Thanks to Ellen Reid, Maxim Fetissenko, PhD, and Laurie-Marie Pisciotta for their help with Keynote.

Below is an approximation of this video’s audio content. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video.

Why does frequent consumption of vegetables appear to cut one’s odds of depression by more than half? And, by more frequent, they mean eating vegetables not three or more times a day, but just three or more times a week. But, even that seemed to cut the odds of developing depression by 60%, after controlling for a long list of variables.

In the 2012 study that found that eliminating animal products improved mood within two weeks, the researchers blamed arachidonic acid—primarily in chicken and eggs, which may adversely impact mental health via a cascade of brain inflammation. But, better moods on plant-based diets could also be from the good stuff in plants—a class of phytonutrients that crosses the blood-brain barrier into our heads. This recent review in the journal Nutritional Neuroscience suggests that eating lots of fruits and vegetables may present “a noninvasive, natural, and inexpensive therapeutic means to support a healthy brain.” Yeah, but how?

Well to understand the latest, we need to understand the underlying biology, the so-called monoamine theory of depression—the thought that depression may arise out of a chemical imbalance in the brain. Here’s the oversimplified version. One of the ways the billions of nerves in our brain communicates with one another is through chemical signals called neurotransmitters. Here’s the end of one nerve, and the beginning of another.

This is what it actually looks like under a microscope. Note the two nerve cells don’t actually touch; there’s a physical gap between them. To bridge that gap, when one nerve wants to tap the other on the shoulder, it releases chemicals into that gap, including three monoamines, serotonin, dopamine, and norepinephrine. These neurotransmitters then float over to the other nerve, to get its attention. The first nerve then sucks them back up, to be reused the next time it wants to talk. But, it’s also constantly manufacturing more, and an enzyme—monoamine oxidase—is constantly chewing them up to maintain just the right amount.

The way cocaine appears to work is by acting as a monoamine reuptake inhibitor. It blocks the first nerve from sucking back up those three chemicals, and so, there’s this constant tapping on the shoulder, this constant signaling to the next nerve. Amphetamines work in the same way, but also increase monoamine release. Ecstasy works like speed, but just causes comparatively more serotonin release.

After a while, the next nerve may be like, enough already, and downregulate its receptors to turn down the volume. It puts in earplugs. So, you need more and more of the drug to get the same effect. And then, when you’re not on the drug, you may feel crappy—because normal volume transmission just isn’t getting through as much.

Antidepressants are thought to work along similar mechanisms. People who are depressed appear to have elevated levels of monoamine oxidase in their brain. That’s the enzyme that breaks down those neurotransmitters. And so, if you have too much of that enzyme in critical parts of your brain—the black circles are the levels in the brains of depressed individuals, and white circles that of the healthy individuals. If your levels of your neurotransmitter-eating enzyme is elevated, then your levels of neurotransmitters drops, and you become depressed, or so the theory goes.

So, a number of different classes of drugs have been developed. The tricyclic antidepressants—named because they have three rings, like a tricycle—appear to block norepinephrine and dopamine reuptake. And so, even though your enzymes may be eating these up at an accelerated rate, what gets released sticks around longer. Then, there came the SSRIs, like Prozac—the selective serotonin reuptake inhibitors. Now, you can know what that means—it just blocks the reuptake of serotonin.

Then, there are drugs that just block the reuptake of norepinephrine. Or, more dopamine. Or, the opposite. But, if the problem is too much high levels of monoamine oxidase, why not just block the enzyme? Make a monoamine oxidase inhibitor. And, of course they did. But, they’re considered drugs of last resort because of serious side effects—not the least of which is the dreaded “cheese effect,” where eating certain foods (like certain cheeses) while on the drug can have potentially fatal consequences. If only there were a way to tamp down the activity of this enzyme, without the whole bleed-into-your-brain thing, and die thing.

Well, now we can finally talk about the latest theory as to why fruits and vegetables may improve our mood. There are inhibitors of that depression-associated enzyme in various plants. There are phytonutrients in spices, such as cloves, oregano, cinnamon, nutmeg. But, people don’t eat enough spices to get enough into the brain. This dark green leafy has a lot, but its name is tobacco—which may actually be one of the reasons cigarettes make smokers feel so good.

Okay, but what if you don’t want brain bleeds or lung cancer? Well, there is a phytonutrient found in apples, berries, and grapes, and kale, onions, and green tea that may indeed affect our brain biology enough to improve our mood.

Please consider volunteering to help out on the site.

Images thanks to practicalowl and gloom via flickr, and Mouagip, Nrets, Dake, ThePallanz, and Savant-fou via Wikimedia. Thanks to Ellen Reid, Maxim Fetissenko, PhD, and Laurie-Marie Pisciotta for their help with Keynote.

Doctor's Note

For more on the inflammatory omega-6 arachidonic acid in chicken and eggs, which may impact mental health via a cascade of brain inflammation, see:

For other natural treatments for mental illness, check out:

Keep up with all of my videos on mood and depression on the topic page

I got some feedback from those who previewed this video on DVD that my explanation of MAO inhibition was a bit much (too complicated). I think there are different camps of NutritionFacts.org viewers. Some who just want to know the bottom line, and others who are fascinated by the underlying mechanisms, and are eager to learn the underlying biology (the “why,” not just the “what” and “how”). I’d be interested in everyone’s feedback. Do these more in-depth explanations add to or detract from the educational value?

For further context, check out my associated blog post: Can We Fight the Blues with Greens?

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